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Carotid Artery Disease

  • Carotid artery disease

    Patho physiology: Carotid artery disease is a disease in which a waxy substance called plaque builds up inside the carotid arteries. You have two common carotid arteries, one on each side of your neck. They each divide into internal and external carotid arteries. The internal carotid arteries supply oxygen-rich blood to your brain. The external carotid arteries supply oxygen-rich blood to your face, scalp, and neck. If plaque builds up in the body's arteries, the condition is called atherosclerosis. Over time, plaque hardens and narrows the arteries. This may limit the flow of oxygen-rich blood to your organs and other parts of your body. Atherosclerosis can affect any artery in the body. For example, if plaque builds up in the coronary (heart) arteries, a heart attack can occur. If plaque builds up in the carotid arteries, a stroke can occur. A stroke also can occur if blood clots form in the carotid arteries. This can happen if the plaque in an artery cracks or ruptures. Blood cell fragments called platelets (PLATE-lets) stick to the site of the injury and may clump together to form blood clots. Blood clots can partly or fully block a carotid artery.

  • Carotid artery disease

    Treatment: Treatments for carotid artery disease may include lifestyle changes, medicines, and medical procedures. The goals of treatment are to stop the disease from getting worse and to prevent a stroke. Making lifestyle changes can help prevent carotid artery disease or keep it from getting worse. For some people, these changes may be the only treatment needed: • Follow a healthy diet to prevent or lower high blood pressure and high blood cholesterol and to maintain a healthy weight. • Be physically active. Check with your doctor first to find out how much and what kinds of activity are safe for you. • If you're overweight or obese, lose weight. • If you smoke, quit. Also, try to avoid secondhand smoke. You may need medicines to treat diseases and conditions that damage the carotid arteries. High blood pressure, high blood cholesterol, and diabetes can worsen carotid artery disease. Some people can control these risk factors with lifestyle changes. Others also need medicines to achieve and maintain control. You may need anticlotting medicines to prevent blood clots from forming in your carotid arteries and causing a stroke. Damage and plaque buildup make blood clots more likely. Aspirin and clopidogrel are two common anticlotting medicines. They stop platelets from clumping together to form clots. These medicines are a mainstay of treatment for people who have known carotid artery disease. You may need a medical procedure to treat carotid artery disease. Doctors use one of two methods to open narrowed or blocked carotid arteries: carotid endarterectomy (END-ar-ter-EK-to-me) and carotid artery angioplasty and stenting.

  • Carotid artery disease

    Research: Screening for concomitant atherosclerotic disease is important in cardiovascular risk reduction. This study assessed the prevalence of carotid artery disease (CAD) and peripheral arterial disease (PAD) in patients with known abdominal aortic aneurysms (AAAs). All patients with AAA attending the vascular laboratory between the January 1, 2007, and December 31, 2009, were eligible for a carotid ultrasound and measurement of ankle brachial indices. A total of 389 (305 males) patients were identified on the AAA surveillance program with a mean (±standard deviation) age of 76 (±8) years. The mean age of the males was 75.4 (±7.8) years, and the mean age of the females was 77 (±11) years. A total of 332 patients were assessed for CAD, and 101 (30.4%) of those were found to have significant disease. A total of 289 patients were assessed for PAD of which 131 (45.3%) were found to have PAD at rest, and 289 patients were assessed for both and 59 (20.4%) patients had significant CAD + PAD. Patients with AAAs are at high risk of other atherosclerotic disorders, and, therefore, they should receive intensive medical optimization

  • Carotid artery disease

    Statistics: In 2001, Medicare announced that it would reimburse hospitals and physicians involved in CAS, but only under an FDA Investigational Device Exemption (IDE). With this landmark decision came the birth of SAPPHIRE (Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy trial).11This was the first FDA-sanctioned trial involving CAS with the simultaneous use of EPDs. The aim of this trial was not to show that stenting is superior to surgery, but that it is not inferior by a difference of 3%. A total of 747 patients were enrolled in this trial. The study protocol randomized high-risk patients defined as: Age greater than 80 years, Severe pulmonary disease, Severe congestive heart failure or concomitant severe coronary artery disease, Contralateral cervical carotid artery occlusion, Unstable angina, arotid stenosis inaccessible to vascular surgeons, Previous radiation therapy in the carotid stenosis site Symptomatic patients with 50% luminal stenosis or asymptomatic patients with 80% luminal stenosis were accepted into this randomized trial. Cardiologists, radiologists, surgeons, and neurologists all participated in the decisions on which patients would be allowed into the trial. Actually, the nonrandomized stent arm (NRSA) of this trial was defined by the surgeons themselves. The EPD used in SAPPHIRE was theAngioguard, by Cordis. The study had 3 arms: • Randomized CEA vs CAS with EPD (334 patients) • Nonrandomized stent arm for patients who were refused surgery (406 patients) • Nonrandomized surgical arm for patients who were refused CAS (7 patients) At 2 years, patients receiving CAS with EPD fared significantly better than those undergoing CEA in the composite endpoint of death, stroke, and myocardial infarction (12.0% vs 20.1%, P<0.05). However, this result was driven primarily by myocardial infarction, because there was no significant difference in death or stroke (the trend still favored CAS). In symptomatic patients, no statistically significant difference existed between the CAS and the CEA groups (16.8% vs 16.5%) (Fig) Again in asymptomatic patients, no difference existed between the CAS and the CEA groups (5.4 vs 10.2, P = 0.20).The Acculink for Revascularization of Carotids in High-Risk Patients (ARCHeR)12 was a prospective trial with CAS and EPD using the RX AccuLink Carotid Stent System and the RX Accunet Embolic Protection System in high-risk surgical patients. This study enrolled, in 3 single-arm trials, 581 patients who met the following criteria: 50% symptomatic stenosis or 80% asymptomatic stenosis with one of the following: Two or more coronary lesions, Severe pulmonary disease, End-stage renal disease, History of neck radiation, Contralateral carotid occlusion, Myocardial infarction in the previous 30 days, Uncontrolled diabetes mellitus. The primary endpoint of death, myocardial infarction, and stroke at up to 2 years in ARCHeR 1 and 2 were 8.3% and 10.2%, respectively. ARCHeR 1 used the Acculink nitinol stent without cerebral protection, whereas Archer 2 used a cerebral protection device. ARCHeR 3 was similar in the usage of the stent and EPD; however, the monorail delivery system was used exclusively during this phase of the trial. Not enough patients in this trial have reached 1 year; therefore, the ARCHeR 3 results are unavailable.

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